Welcome to our list of myths and misconceptions in physio! This list is designed for students, but it might be useful for qualified physios, too. There are seven sections of myths and misconceptions: assessment, treatment, clinical reasoning, condition-specific, exercise, pain science, and evidence based practice.

Why did I write this list? Well, as students, my friends and I spent a lot of time and energy working this stuff out. I want to save future students from having to do all that frustrating work, so they can concentrate on learning new things.

Postural, structural and biomechanical quirks show you the cause of pain

Structure is not destiny! Pelvic tilt, lordosis, kyphosis, ‘over’ pronation, weak muscles, tight muscles, bulging discs, asymmetries, mild scoliosis: these things do not explain pain and worrying about them can feed in to more pain.

Postural types are scientific

They’re really pseudo-scientific, and posture correction has a long and ignoble history. The idea that we should sit and stand up straight is simply made up

Scans show you the cause of pain

Treat the man, not the scan! Brinjikji et al found that people with no pain have all sorts of things going on in their spines. This doesn’t mean the scan is irrelevant, just that it is part of a complex picture.

Core instability causes back pain

The one myth to rule them all. Peter O’Sullivan produced some of the research that started the core stability myth, and now totally refutes its value as an explanation of LBP. His youtube videos show his new approach.Ben Smith’s systematic review is the most recent of many to indicate that core stability training is no better than any other exercise for LBP. This podcast is a nice intro to his work. Telling someone their core needs stabilising is just plain mean.

Is this in danger of becoming a new myth? Good hands are important for performing certain special tests, for manual therapy, and for communicating with your patient and making them feel safe. We are one of the only professions that gets to use touch to reduce people’s pain, help them move and build their strength and confidence.

Massage increases blood flow and has all sorts of effects on soft tissues

Massage probably does increase superficial, cutaneous blood flow (making skin look red). But it’s unlikely it does anything to the blood flow of deeper tissues.Massage is great but probably not because it is causing meaningful changes in soft tissues such as lengthening or aligning them, or washing out inflammation.

Manual therapy works by “pain gate” theory

This theory was put forward by Melzack and Wall in 1965 and is very significant in the history of pain science because it was the first theory to account for top-down modulation of pain (ironically the bit that is most forgotten when people think of Pain Gate now). But it is such a small part of a complex picture that some time ago Melzack and Wall encouraged people to move on.

Joint mobilisations/manips put the joint back in place

The mechanisms of manual therapy are mostly “neurophysiological”. Whether or not “neurophysiological” mechanisms are specific to manual therapy is up for debate.

Manual therapy is direction specific

All pressure applied onto the skin is transferred perpendicularly through bone and soft tissue because the skin-fascia interface is frictionless. Here is an adorable video to explain this. This means that pulling, pushing and grabbing anything except skin in any particular direction is not going to happen.

Sometimes we tell people in pain to “pace yourself”. Often, this is heard as “do what you feel able to do”. In fact, pacing is about doing the same, manageable amount daily, regardless of how you feel, and increasing over time.

It is human nature to want to try every tool in the toolkit to help someone in pain. But often this approach forgets that as well as potential benefits, all treatments have costs. This may be in terms of time and money, which is an important consideration if you work in the NHS, but more importantly they may be in the form of harm to the patient. All treatments have the potential to rob patients of their self-efficacy and to encourage maladaptive beliefs and behaviour.

There are responders and non-responders to treatments

The idea that certain people “respond” to certain treatments is appealing, and it is nice to think that there is a perfect patient for each tool in your toolkit. Unfortunately, data suggest that for our underwhelming pain treatments, including exercise, there is no hidden group of responders.

Placebo is a powerful force that we need to leverage

The debates about placebo are endless but it is sufficient to say that we should be wary of anyone saying that placebo is 1) powerful or 2) something we need to “leverage” with complicated extra interventions. The fact is that placebo is 1) a limited, unreliable, unpredictable thing and 2) the best part of placebo can be obtained through patient therapist interaction without the need for needles or machines.

Condition-specific myths and misconceptions

Myth

Explanation

OA is wear and tear

OA is a metabolically active process, so telling a patient they have “wear and repair” rather than “wear and tear” is not only less fear inducing but more truthful.

Tea and juice are in fact more hydrating than water, so it’s okay for people with, for example, bronchiectasis to drink these things.

Shoulder impingement is a thing

It’s not a thing. Neer’s model of shoulder impingement doesn’t really hold up and might be fear-inducing for patients. Is it better to say that weak and painful shoulders have “rotator cuff tendinopathy”? Any ‘impingement’, in this case, is secondary and not a diagnosis.

Running causes OA

Evidence is conflicting and common sense suggests that well-managed loading is good for joints, so we can challenge patients’ beliefs that running causes “wear and tear”.

There aren’t articular adhesions, so some say it might be better to call this condition “frozen shoulder contracture syndrome”. And since there are no adhesions to break down, it makes little sense to bring patients in for aggressive range-of-motion exercises.

Exercise myths and misconceptions

Myth

Explanation

Stretching causes muscles to lengthen

This is possible but takes a lot of force and time, and it’s unlikely that even a good long yoga session is enough to stimulate actual tissue changes – even in terms of tissue flexibility. Instead what is likely to be adapting is the nervous system, which is ‘reassured’ by stretching that the end range of motion is safe, and therefore ‘allows’ the muscle to lengthen a bit more next time. **EDIT** Is this myth a myth? Update coming!

Some physios have accepted that pain isn’t in the tissues and decided it must be in the brain instead. But, it’s not there either. Whether or not saying “pain is in the brain” is a helpful thing to say to patients is debatable.

There are “pain signals” that travel along “pain fibers”

“Eyes have light receptors, not vision. Ears have vibration receptors, not hearing. Tissue has danger receptors, not pain” — Adrian Louw. Pain is an output of the brain.

People in persistent pain have got central sensitization

Central sensitization, the long-term potentiation of pain in the spinal cord and brain, is often assumed to be inevitable if someone has been in pain for a long time. But central sensitization isn’t just another word for persistent pain, it’s its own particular thing. So, someone with chronic low back pain may or may not have central sensitization. This story illustrates one unexpected danger of assuming persistent pain is centrally driven.

Explaining pain is about teaching people to manage pain

There are many educational interventions that help people to cope with pain, but pain neuroscience education is about reducing pain.

Pain science relegates the “bio” from the “biopsychosocial”.

Pain science does not imply that bio-factors, including biomechanics, are irrelevant – it just puts them in a better context. Indeed, pain neuroscience education has not yet been shown in an RCT to reduce pain without some kind of exercise or manual therapy intervention to go with it.

Pain science is for persistent pain.

Many patients can benefit from the message that hurt does not equal harm.

A result can be statistically significant but meaningless for your patient. Look at the raw data, the effect size, minimal clinically important difference, and so on. And raise an eyebrow whenever a trial’s results are simply reported as “significant”.

The P-value is the probability that your results occurred by chance

The P-value is the likelihood that chance could throw up your results even if there was no difference between treatments. The problem with this is that, in most things, it’s far more likely that there is indeed no difference than a real difference, meaning that you get a lot more false positives than you might expect. Add to this the fact that most studies are powered to find only 80% of true positives anyway, and false-positives hugely outweigh true ones. This is called the base rate fallacy. For example, even in a trial where the probability of there being a real effect is 50:50, a very high estimate, “P=<0.05” means that the false-positive rate is 26%.

A sample needs to be representative for a study to be relevant

Commonly, you will hear results of trials dismissed because the sample does not represent a clinical population. While it is true that a representative sample helps to generalise findings, it can also undermine them. Representative samples have lots of confounding variables that reduce the internal validity of a trial. This means that external validity and internal validity become a see-saw. If a trial appears weak because its sample is not representative, it may be that its greater internal validity more than makes up for this.

The stool metaphor implies that all three legs – research, clinical experience and patient preference – have equal value when making clinical decisions. But they don’t.

Small studies are unlikely to have false positives.

It is well known that small studies are worse at detecting true effects; that is, they make more type II errors. Often people take this to mean that if small studies do show an effect then that effect is more likely to be real. In fact, small studies are also more likely to show a false effect; that is, they make more type I errors, proportionately, than large studies, because there aren’t as many real effects to water them down.

I admire the amount of work and effort that has gone into this. I suspect its like a fantastic chocolate tort, amazing on the first few bites but too rich to have this much a slice in one serving. I love the metabolic link for OA, its taken me 15 years to stumble across that one but if metabolic and genetic which is my belief for the present, I’m not sure “wear” is also an appropriate term.
Also while posture cannot explain back and shoulder pain, if altering it helps the person then Jeremy Lewis SSMP model for exaple certainly allows for this to form as significant part of the rehab that it requires? lets not throw it all away if its helpful or why bother strenghtening anything if we dont need the muscle for power of posture and if muscle cant explain pain?
My interpretation of Mick Thackers Paradigm model would also suggest we need to fit into the persons reality or paradigm of their pain and altering this to fit our “professional understading of today” may be folly. Belief as we all know is powerful and unless their belief system is hareful why take it away if it leaves them in mental limbo. this in itself is a form of harm.
“When chronic pain is not Chronic pain by Alan Taylor and Roger Kerry give us pertinent lessons to not believe too strongly in what we think now and what we will think in the future.
just my ramblings but I admire the blog, well done

Thanks Tony for your thoughtful comments. I do agree with all of them – I presented this article to have impact, which it has done, but it does mean some subtlety has been lost along the way. I particularly like your comment about ‘fitting into the person’s reality’ – it’s no good imposing our world view on others and bulldozing over theirs. I think this is what Quinter & Cohen mean by the “third space” and Edwards has written about matching the “pain schema” of the patient to your own. Very hard to do and as a novice Physio I’m not sure I’ve managed yet and sometimes find myself “explaining pain” by rote, which I never like. Thanks again for the comments.